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At least 19 recordsLinked to original sources
PubMed1979

Adrenocortical function tests in dogs with hyperfunctioning adrenocortical tumours.

The response has been studied in nine dogs with hyperadrenocorticism due to adrenocortical tumours to the administration of dexamethasone, insulin, lysine-vasopressin and tetracosactide by measuring the changes in plasma cortisol concentration. Administration of dexamethasone did not produce a decrease in the plasma concentration of cortisol in any of these dogs. Administration of insulin caused slight increases in the plasma concentration of cortisol in four out of eight dogs. Lysine-vasopressin increased the plasma concentration of cortisol in eight out of nine dogs, three responded supranomally. Eight out of the nine dogs responded to tetracosactide administration, three responded supranormally, It is concluded that in the dog, in contrast to man, the lysine-vasopressin test cannot be used to differentiate between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to an adenocortical tumour. Apparently pituitary ACTH is not completely depleted in dogs with hyperfunctioning adrenocortical tumours.

Adrenal Cortex Function Tests↗
PubMed1990

Assessment of survey radiography and comparison with x-ray computed tomography for detection of hyperfunctioning adrenocortical tumors in dogs.

Results of abdominal survey radiography and x-ray computed tomography (CT) were compared in 13 dogs with hyperadrenocorticism histologically attributed to adrenocortical tumors. X-ray computed tomography enabled accurate localization of the tumor in all 13 dogs. Apart from 2 poorly demarcated irregular-shaped and mineralized carcinomas, there were no differences between adenoma (n = 3) and carcinoma (n = 10) on CT images. In 1 dog, invasion of the caudal vena cava by the tumor was suggested on CT images and was confirmed during surgery. Suspicion of adhesions between tumors of the right adrenal gland and the caudal vena cava on the basis of CT images was confirmed during surgery in only 2 of 6 dogs. Survey radiography allowed accurate localization of the tumor in 7 dogs (4 on the right side and 3 on the left). In 6 of these dogs, the tumor was visible as a well-demarcated soft tissue mass and, in the other dog, as a poorly demarcated mineralized mass. The smallest tumor visualized on survey radiographs had a diameter of 20 mm on CT images. Six tumors with diameter less than or equal to 20 mm were not visualized on survey radiographs. In 1 of these dogs, a mineralized nodule was found in the left adrenal region, without evidence of a mass. In a considerable number of cases, survey radiography can provide presurgical localization of adrenocortical tumors in dogs with hyperadrenocorticism; CT is redundant in these instances. In the absence of positive radiographic findings, CT is valuable for localization of adrenocortical tumors.

Adenoma↗
PubMed1977

HLA antigens in patients with adrenocortical hyperfunction.

The HLA antigen frequencies in 100 Caucasian patients with adrenocortical hyperfunction were compared with those found in 352 healthy unrelated subjects. Fourteen antigens on the HLA--A locus, seventeen antigens on the HLA--B locus and three antigens on the HLA--C locus were determined using the standard NIH microlymphocytotoxicity test. The frequency of HLA--A1 antigen in the patient group was 49% as compared with 28% in the controls (pcorr less than 0.01). An increased frequency of HLA--B8 and HLA-BW35 antigens was also found, but the difference was not significant. Increased A1--B8 and A1--BW35 haplotype frequencies were observed. The relationship between the HLA system and various endogenous and exogenous factors eliciting hypercorticism, together with complementary family studies indicate that the HLA system may be a useful genetic marker of the disease susceptibility gene.

Adrenocortical Hyperfunction↗
PubMed1990

Nephrotomography and ultrasonography for the localization of hyperfunctioning adrenocortical tumors in dogs.

Nephrotomography and ultrasonography were used in 11 dogs with hyperadrenocroticism to assess the value of these techniques for the localization of biochemically diagnosed hyperfunctioning adrenocortical tumors. Both techniques enabled accurate localization of a unilateral adrenal mass in each of the dogs. Cross-sectional diameters of the masses ranged from 1 to 4 cm. In 1 dog, expansion of tumor into the caudal vena cava was revealed by caudal venacavography and ultrasonography. Mineralization in the tumor mass in 2 dogs was easily recognized by nephrotomography, but not by ultrasonography. Paracostal laparotomy confirmed the presence of an adrenocortical tumor in each dog, and expansion of tumor into the caudal vena cava in 1 dog. Cross-sectional diameters of the tumors ranged from 1.2 to 4.5 cm and corresponded well with cross-sectional measurements by nephrotomography and ultrasonography. It was concluded that nephrotomography and ultrasonography have similar diagnostic accuracies for the detection and localization of hyperfunctioning adrenocortical tumors.

Adrenal Cortex Neoplasms↗
PubMed1992

Corticoid production by four dogs with hyperfunctioning adrenocortical tumours during treatment with mitotane (o,p'-DDD).

In two dogs with hyperadrenocorticism due to an adrenocortical tumour, treatment with o,p'-DDD was started. Their hormonal response was monitored by measurements of the urinary corticoid/creatinine ratio. In one dog, two courses of 10 days treatment with o,p'-DDD were ineffective, whereas in the other dog the urinary corticoids decreased to very low levels after only six days of treatment, and corticosteroid supplementation had to be started. Two other dogs received o,p'-DDD according to a protocol used for the treatment of pituitary-dependent hyperadrenocorticism which aims at the complete destruction of the adrenal cortices, with substitution for the induced hyperadrenocorticism. Both dogs made a good recovery and their urinary corticoid/creatinine ratio decreased to within the reference range. In one of them the tumour had decreased considerably in size by five weeks after the start of the treatment.

Adenoma↗
PubMed1991

Osmoregulation of systemic vasopressin release during long-term glucocorticoid excess: a study in dogs with hyperadrenocorticism.

In 9 dogs with pituitary-dependent hyperadrenocorticism and in 6 dogs with hyperfunctioning adrenocortical tumours, the osmoregulation of arginine vasopressin (AVP) release was investigated by iv infusion of 20% NaCl for 2 h at a rate of 0.03 ml per kg body weight. The responses were analysed in terms of sensitivity and threshold of the osmoregulation of AVP secretion. The sensitivity was normal in 6 dogs and lowered in 9. In 4 of the latter dogs there was complete absence of a response to hypertonicity. The osmotic threshold of AVP release was raised in 9 dogs and normal in 2 dogs, whereas in the four dogs without any response the term threshold was not applicable. The results were not different for dogs with pituitary-dependent hyperadrenocorticism and dogs with hyperfunctioning adrenocortical tumour. It is concluded that corticosteroid excess per se induces a marked impairment of the osmoregulation of AVP secretion. The loss of reactivity of the osmoreceptor system may contribute to the corticosteroid-induced polyuria, which is also the result of resistance to AVP in the kidney.

Adrenal Cortex↗
PubMed1978

The prevalence of antibodies against Toxoplasma gondii among hospitalized animals and stray dogs.

Hospitalized animals and stray dogs were serologically tested for antibodies against Toxoplasma gondii. In addition, the data were examined for the possibility of toxoplasmosis infection being associated with the clinical diagnosis and with the discharge status (alive vs. dead). Among 1056 hospitalized animals, 17 (20%) of 86 cats, 112 (14%) of 804 dogs, 34 (26%) of 133 horses and 6 (18%) of 33 cattle had serological evidence of infection with T. gondii. Only 22 (6%) of 342 young (median age = one year) stray dogs were seropositive. The difference in antibody prevalence between hospitalized and stray dogs was thought to be due to age and dietary factors. Of 249 dogs grouped by clinical diagnosis, there was significantly (p less than 0.01) higher prevalence of seropositives among dogs with diseases of the kidney or with adrenocortical hyperfunction than among dogs hospitalized for other diseases. Of 19 dogs with diseases of the kidney and 12 with adrenocortical hyperfunction 37% and 42%, respectively, were seropositive.. There was higher risk of being discharged from the hospital dead among seropositive dogs, cattle and horses than among seronegative animals of the same species. The exception was cats, where of 69 seronegative cats 29% were dead at discharge and where of 17 seropositive cats 18% were dead at discharge. The possible effects of stress due to hospitalization need further research.

Animals↗
PubMed1979

Evaluation of steroid laboratory tests and adrenal gland imaging with radiocholesterol in the aetiological diagnosis of Cushing's syndrome.

Basal values of the urinary excretion of 17-oxogenic steroids and serum levels of cortisol were not satisfactory in the differentiation of 'suspected' subjects from patients with true Cushing's syndrome. With an RIA method for serum cortisol determination, the overnight dexamethasone suppression test provided the most reliable single test in establishing adrenocortical hyperfunction. Thirty-five normal subjects, fifty-nine obese patients, thirteen 'suspected' patients, and thirteen patients with disease states other than Cushing's syndrome had suppressed values below 4.0 microgram/100 ml. None of the ten patients with Cushing's syndrome had a cortisol concentration less than 16.3 microgram/100 ml. Adrenal gland scintigraphy after radiocholesterol injection is a more valuable tool than the metyrapone test and the high-dose dexamethasone suppression test in the localization and differential diagnosis of adrenocortical lesions causing Cushing's syndrome. It obviates the need for angiographic procedure in the localization of adenomas. It is a reliable technique for identifying functioning adrenal remnants. We therefore propose a schedule for studying patients with suspected adrenocortical hyperfunction.

17-Ketosteroids↗
PubMed1975

Studies on ectopic ACTH-producing tumors. II. Clinical and biochemical features of 30 cases.

This report describes the clinical and biochemical features of 30 cases of ectopic ACTH-producing tumors diagnosed by the detection of ACTH in the tumor tissues. Several uncommon tumors, such as tumors of the esophagus, stomach, and larynx, were included in this series. None of the patients with bronchogenic carcinoma showed signs of classical Cushing's syndrome, whereas 7 of the remaining 13 patients with other tumors were Cushingoid in appearance. Adrenocortical hyperfunction was present in 61 percent at the first examination and developed during the course of the disease in 18 percent more. In the remaining patients (21 percent), adrenocortical function remained within normal limits. These results indicate that there exist ectopic ACTH-producing tumors without clinical and biochemical sequelae of excess hormone. In some of the tumor extracts studied, MSH and CRF-like activities and serotonin were detected. This suggests that multiple hormone production is not uncommon in ectopic ACTH-producing tumors.

Adrenocortical Hyperfunction↗
PubMed1990

[Immunoreactive trypsin in the blood of patients with functional disorders of the adrenal cortex].

Blood serum trypsin was radioimmunoassayed in 46 patients with adrenocortical hyperfunction and in 24 ones with its hypofunction. The findings evidence that excess of endogenous adrenal steroids leads to elevation of radioimmune trypsin (RIT) concentration. The presence of chronic pancreatitis in hypercorticism did not essentially influence the value of the examined parameter, nor did the development of diabetes mellitus. Corticosteroid deficit in the body was not associated with changes in the blood serum RIT concentration. Systematic glucocorticoid therapy resulted in elevation of RIT level. The serum enzyme concentration was also increased in hypoadrenocorticism patients not administered glucocorticoids, suffering from concomitant chronic pancreatitis. Therefore the test was not informative for the diagnosis of chronic pancreatitis in the patients with the endogenous hyperadrenocorticism syndrome but may be helpful in the recognition of the condition in the patients with chronic adrenal insufficiency; interpretation of this test results in hypoadrenocorticism patients treated with glucocorticoids should be performed by efficient specialists.

Adolescent↗
PubMed1979

Gastrinoma associated with common bile duct obstruction and the ectopic production of ACTH.

A case of adrenocortical hyperfunction due to ectopic production of ACTH by a gastrin-producing tumor of the pancreas is described. Cushing's syndrome preceded the appearance of the overt Zollinger-Ellison syndrome by 2 years and was treated by bilateral adrenalectomy. The Zollinger-Ellison syndrome was initially treated with cimetidine, which successfully reduced the secretion of gastric acid. Because the pancreatic gastrinoma continued to grow, causing obstruction of the common bile duct, biliary diversion and total gastrectomy were performed. There is evidence that the pancreatic gastrinoma was the source of the ectopic production of ACTH and possibly secretion. The role of Histamine-2 blocking agents as therapy in the Zollinger-Ellison syndrome is discussed.

Adrenocorticotropic Hormone↗
PubMed1992

Clinical features of depressed patients who do and do not improve with placebo.

The substantial placebo response in depression confounds treatment decisions and the assessment of new therapies. Improvement with placebo occurs infrequently in patients with chronic depression and in those with pituitary-adrenocortical hyperfunction, but other consistent predictors of placebo response have not been detected. We divided 241 moderately to severely depressed patients who had received placebo on a double-blind basis for 3 to 6 weeks into responders (greater than or equal to 50% improvement in Hamilton depression score, final Hamilton depression score less than or equal to 10), extreme nonresponders (less than 25% improvement), and partial responders (all others). Improvement with placebo was associated with a relatively short illness, a precipitating event, depression of only moderate global severity, and a good response to previous antidepressant treatment. These observations suggest that depressed patients who do and do not recover with placebo have different conditions that have not yet been fully characterized.

Adult↗